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Anosognosia for hemiplegia (AHP) is informative about the neurocognitive basis of motor awareness. However, it is frequently associated with concomitant symptoms, such as hemispatial neglect and disturbances in the sense of body ownership (DSO). Although double dissociations between these symptoms have been reported, there is ongoing debate about whether they are manifestations of independent abnormalities, or a single neurocognitive deficit. We aimed to investigate the specificity of lesions associated with AHP by surpassing four, existing methodological limitations: (a) recruit a relatively large sample of patients (total N = 70) in a multi-centre study; (b) identify lesions associated with AHP in grey and white matter using voxel-based methods; (c) take into account the duration of AHP and concomitant neglect symptoms; and (d) compare lesions against a control hemiplegic group, patients suffering from AHP and DSO, and a few, rare patients with selective DSO. Results indicated that acute AHP is associated with a wide network, mainly including: (1) the Rolandic operculum, (2) the insula and (3) the superior temporal gyri. Subcortically, damage mainly involved the basal ganglia and white matter, mostly the superior corona radiate, arcuate fasciculus and the part of the ventral, superior longitudinal fasciculus. Persistent symptoms were linked with wider damage involving fronto-temporal cortex and long white matter tracts. A shift in the latero-medial direction (mainly involving the basal ganglia and surrounding white matter) emerged when DSO was taken accounted for. These results suggest that while bodily awareness is processed by areas widely distributed across the brain, intact subcortical structures and white matter tracts may be necessary to support basic feelings of owning and controlling contralateral body parts. An accurate and 'up-to-date' awareness of our motor abilities, however, may rely also on intact processing in cortical areas which presumably allow higher-order inferences about the current state of the body., (Copyright © 2016 Elsevier Ltd. All rights reserved.)

Objective: According to a still-controversial view of recognition, projections between the perirhinal cortex and the medial subdivision of the mediodorsal thalamic nucleus (mMDT) support the mnemonic processes underlying familiarity, whereas a separate extended hippocampal system is critical for the recollection of episodic details during recognition., Method: In this study, we examined item recognition, familiarity, and recollection for faces and words in a patient (OG) with a right-sided lesion centered on the mMDT, which encroached on the central medial midline nucleus and may have resulted in partial disconnection of the mammillothalamic tract. On the basis of OG's neuropathology, the dual-process signal-detection (DPSD) high-threshold theory and the material-specific hypothesis of long-term memory together predicted a material-specific impairment in familiarity for novel facial memoranda, with a lesser decline in recollection of novel faces at short retention intervals. No abnormalities in either familiarity- or recollection-driven recognition of verbal memoranda were expected., Results: Comparing the performance of OG and that of a group of 10 age-, sex-, and IQ-matched healthy controls, the remember-know procedure revealed the dissociations predicted by the material-specific and DPSD hypotheses: With recognition of previously novel faces, OG showed a deficit in familiarity-driven recognition that was significantly greater than the insignificant reduction in his recollection. All components of his word recognition were, however, preserved., Conclusion: A memory profile, marked by a dissociation between familiarity and recollection, fits naturally with the DPSD model and is incompatible with the idea that these kinds of memories reflect different degrees of trace strength., (PsycINFO Database Record (c) 2016 APA, all rights reserved.)

Medicated, non-dementing mild-to-moderate Parkinson's disease (PD) patients usually show recall/recollection impairments but have only occasionally shown familiarity impairments. We aimed to assess two explanations of this pattern of impairment. Recollection typically improves when effortful planning of encoding and retrieval processing is engaged. This depends on prefrontally-dependent executive processes, which are often disrupted in PD. Relative to an unguided encoding and retrieval of words condition (C1), giving suitable guidance at encoding alone (C2) or at encoding and retrieval (C3) should, if executive processes are disrupted, improve PD recollection more than control recollection and perhaps raise it to normal levels. Familiarity, being a relatively automatic kind of memory, whether impaired or intact, should be unaffected by guidance. According to the second explanation, PD deficits are amnesia-like and caused by medial temporal lobe dysfunction and although poorer recollection, which is caused by hippocampal disruption, may be improved by guidance, it should not improve more than control recollection. Familiarity impairment will also occur if the perirhinal cortex is disrupted, but will be unimproved by guidance. Without guidance, recollection/recall was impaired in thirty PD patients relative to twenty-two healthy controls and remained relatively equally impaired when full guidance was provided (C1 vs C3), both groups improving to broadly the same extent. Although impaired, and markedly less so than recollection, familiarity was not improved by guidance in both groups. The patients showed elevated rates of subclinical depressive symptoms, which weakly correlated with recall/recollection in all three conditions. PD executive function was also deficient and correlated with unguided/C1 recollection only. Our results are consistent with a major cause of the patients' recall/recollection impairments being hippocampal disruption, probably exacerbated by subclinical depressive symptoms. However, the results do not exclude a lesser prefrontal cortex contribution because patient executive functions were impaired and correlated solely with unguided overall recollection., (Copyright © 2015 Elsevier Ltd. All rights reserved.)

Anarchic hand syndrome (AHS) is characterized by goal-directed movements performed without volitional control (agency). Different AHS subtypes have been identified; however, few studies have examined the posterior subtype. We report a case of AHS following right-hemisphere parietal damage, with left-sided somatosensory and proprioceptive impairment. Agency was examined for nonanarchic (volitional) movements performed using the anarchic hand. The patient experienced abnormal agency for movements whether motor intention and visual feedback were congruent or incongruent, but not when intention was absent (passive movement). Findings suggest a general disturbance of veridical motor awareness and agency in this case of parietal AHS.

This study reports a patient, OG, with a unilateral right-sided thalamic lesion. High resolution 3T magnetic resonance imaging revealed damage to the parvicellular and magnocellular subdivisions of the dorsomedial thalamus (DMT), the central lateral intralaminar nucleus (also known as the paralamellar DMT), the paraventricular and the central medial midline thalamic nuclei. According to the neuropsychological literature, the DMT, the midline and intralaminar thalamic nuclei influence a wide array of cognitive functions by virtue of their modulatory influences on executive function and attention, and this is particularly indicated under conditions of low arousal or high cognitive demand. We explored this prediction in OG, and compared his performance on a range of low and high demand versions of tests that tapped executive function and attention to a group of 6 age- and IQ-matched controls. OG, without exception, significantly under performed on the high-demand attention and executive function tasks, but performed normally on the low-demand versions. These findings extend and refine current understanding of the effects of thalamic lesion on attention and executive function.

A selective deficit in the recollection of episodic details is frequently reported in Parkinson's disease (PD). Previous explanations implicate dopamine dysregulation in prefrontal structures on which strategic memory processes rely. However, neuroimaging advancements suggest dopaminergic dysregulation of hippocampally dependent memory processes. Accordingly, dopamine agonists, which target D3 receptors in the hippocampus, may impair hippocampal functioning, causing a more pronounced recollection decline. Recognition memory (RM), familiarity, and recollection were examined in 21 patients with mild-to-moderate PD (Hoehn and Yahr mean: 2.67). Patients were subdivided into two subgroups according to dopamine agonist (pramipexole [PPX] or ropinirole [RPR]), and completed matched versions of an RM test in a medicated and unmedicated condition (termed ON and OFF, respectively). Ten demographically matched healthy volunteers (HVs) also completed both RM tasks in two separate sessions. The PD group (PPX and RPR subgroups combined) showed impairments in RM and recollection, but spared familiarity. When subdivided by dopamine agonist, the PPX subgroup's ON-medication recollection performance was significantly lower than that of both the HVs and RPR subgroup. There was no evidence of decline in OFF-medication recollection or familiarity in either the PPX or RPR subgroups. Recollection in both PD subgroups correlated positively with a composite measure of recall, but not prefrontally dependent measures of cognitive control. These findings suggest that mild-to-moderate PD patients may show relatively preserved recollection and familiarity, but that recollection is selectively disrupted by PPX, but not RPR and that this effect may depend on disrupted hippocampal function rather than impaired pre-frontally dependent executive functions., (© 2013 The British Psychological Society.)

Neuropsychological findings suggest material-specific lateralization of the medial temporal lobe's role in long-term memory, with greater left-sided involvement in verbal memory, and greater right-sided involvement in visual memory. Whether material-specific lateralization of long-term memory also extends to the anteromedial thalamus remains uncertain. We report two patients with unilateral right (OG) and left (SM) mediodorsal thalamic pathology plus probable correspondingly lateralized damage of the mammillo-thalamic tract. The lesions were mapped using high-resolution structural magnetic resonance imaging and schematically reconstructed. Mean absolute volume estimates for the mammillary bodies, hippocampus, perirhinal cortex, and ventricles are also presented. Estimates of visual and verbal recall and item recognition memory were obtained using the Doors and People, the Rey Complex Figure Test, and the Logical Memory subtests of the Wechsler Memory Scales. Each patient's performance was compared to a group of healthy volunteers matched for demographic characteristics, premorbid IQ, and current levels of functioning. A striking double dissociation was evident in material-specific long-term memory, with OG showing significant impairments in visual memory but not verbal memory, and SM showing the opposite profile of preserved visual memory and significantly impaired verbal memory. These impairments affected both recall and item recognition. The reported double dissociation provides the strongest evidence yet that material-specific lateralization of long-term memory also extends to the anteromedial thalamus. The findings are also discussed in relation to proposals that distinct anatomical regions within the medial temporal lobe, anteromedial thalamus, and associated tracts make qualitatively different contributions to recall and item recognition., (©2011 The British Psychological Society.)

The effect of disease severity and dopaminergic medication on the assessment of familiarity and the recollection of episodic details during recognition in nondementing idiopathic Parkinson's is uncertain. Some studies have reported familiarity as deficient in mild Parkinson's yet others have found it intact even in moderate Parkinson's. Recollection has been found to be both preserved and deficient in mild and moderate Parkinson's. The extent to which these conflicting findings are explained by disease severity or dopaminergic medication or a combination of the two is uncertain, as all studies assessed patients in a medicated state, and disease severity has not always been consistently reported. Twelve patients with mild Parkinson's and 11 with moderate Parkinson's (medicated Hoehn and Yahr mean: 2.1 and 3.2, respectively), completed matched versions of a yes/no recognition memory test in a medicated and unmedicated condition (termed ON and OFF, respectively). Twenty-one matched healthy volunteers also completed both memory tasks in 2 separate sessions (termed Blue and Green, respectively). In the ON/Green condition, the moderate Parkinson's recollection performance was significantly poorer than the healthy volunteers and mild Parkinson's. By contrast, recognition memory and familiarity measures in both Parkinson's group were relatively spared. In the OFF/Blue condition, the moderate Parkinson's recollection was impaired, but only in relation to the healthy volunteer set. There were no significant differences in recollection performance between the mild and moderate Parkinson's groups. Again, recognition memory and familiarity measures in both Parkinson's group were relatively spared. Further analyses showed the moderate patients' recollection rates to be significantly poorer ON-medication compared to OFF. These findings are discussed in relation to the staging of disease progression on medial temporal areas which separately support recollection and familiarity, and the putative effects the different classes of dopaminergic drugs may have on these areas., ((c) 2009 Elsevier Ltd. All rights reserved.)

Neuropsychological research suggests that recognition memory (RM) and recall memory are impaired in patients with a major depressive disorder or a dysphoric mood state. This study examines the proposal that abnormalities in recollection (a form of recall) result from a breakdown in frontal strategic memory processes involved in encoding and retrieval, and executive functions linked to reality monitoring, planning, problem-solving, reasoning and decision-making. We investigated two predictions arising from this theory. Firstly, patients diagnosed with a major depressive disorder (MDD) will display a dissociation between (deficient) recollection and (preserved) familiarity. Secondly, if recollection impairments are indicative of a breakdown in prefrontal strategic memory processes which are dependent, at least in part, on executive processes, then an explicit correlational approach predicts that recollection will be positively associated with the severity of executive dysfunction in MDD patients. The remember/know paradigm was used to investigate RM for words and neutral faces in 16 MDD patients and 16 healthy volunteers, matched for age, gender and estimates of premorbid IQ. Measures of executive function included working memory, reasoning and decision-making. Applying the Dual Process Signal Detection interpretation of the remember/know data, the MDD group displayed significant impairments in RM and recollection rates for both verbal and neutral facial memoranda. In contrast, familiarity-aware rates were preserved. There was no evidence of executive dysfunction in the patient group, and little evidence that recollection rates correlated with executive function. Furthermore, a single process signal detection approach suggested that the MDD patients displayed a reduction in sensitivity for RM and remember rates but not know responses. The criteria for detecting studied from unstudied items, and remembering from knowing, were the same in both patient and healthy control groups. Taken together, these findings are consistent with the view that MDD is marked by a decline in RM, which is underpinned by an impairment in recollection rather than familiarity processes. The extent to which the recollection deficiencies arise from disruption of strategic memory and executive processes requires further investigation., (2008 Elsevier Ireland Ltd. All rights reserved.)

Anosognosia for hemiplegia (AHP) is a lack of awareness about paralysis following stroke. Recent explanations use a 'forward model' of movement to suggest that AHP patients fail to register discrepancies between internally- and externally-generated sensory information. We predicted that this failure would impair the ability to recall from memory whether information is internally- or externally-generated (i.e., reality monitor). Two experiments examined this prediction. Experiment 1 demonstrated that AHP patients exhibit a reality monitoring deficit for non-motor information (i.e., perceived vs. imagined drawings), whilst hemiplegic controls without anosognosia (nonAHP) perform like age-matched healthy volunteers (HVs). Experiment 2 explored if this deficit occurs when AHP patients discriminate performed, imagined, or observed movement. Results showed impaired reality monitoring for movements in AHP and nonAHP patients relative to HVs. Findings suggest that reality monitoring processes not directly related to movement, together with a failure to reality monitor movements, contribute to the pathogenesis of AHP.

Objective: To test the hypothesis that anosognosia for dyskinesias in Parkinson disease (PD) results from a failure to detect discrepancies between intended and actual movement., Background: PD patients often complain of drug-induced dyskinesias (involuntary movements) less than their carers. This remarkable unawareness is an example of anosognosia (ie, unawareness of deficits associated with an illness). A better understanding of anosognosia for dyskinesias in PD is important to understand the impact of the illness and side effects of treatment., Methods: The ability to detect a discrepancy between intended movement and visual feedback about actual movement was investigated in 6 PD patients with anosognosia for dyskinesias, 11 nonanosognosic PD controls with dyskinesias, and 22 healthy volunteers, using a mirror to reverse the expected visual consequences of an executed movement., Results: Nonanosognosic PD patients and healthy volunteers rated mirror-reversed movement as significantly stranger than normal movement (P=0.024 and <0.001, respectively), whereas PD patients with anosognosia for dyskinesias did not (P=0.375)., Conclusions: The findings support our proposal, in that PD patients with anosognosia for dyskinesias do not report mirror-reversed movement (in which intentions and visual feedback conflict) as feeling distinct from normal movement.

Anosognosia for hemiplegia (AHP) is characterised by poor insight or underestimation of hemiplegia after brain injury. Recent explanations of AHP have used an established 'forward model', which proposes that normal motor awareness involves comparing the predicted and actual sensory consequences of movements. These accounts propose that AHP patients may be able to form representations of their intended movements (i.e., motor representations), but fail to register discrepancy between intended and actual movements. A prediction arising from this proposal is that AHP patients are able to generate motor representations involving their hemiplegic limb(s). Our study provides the first direct examination of this prediction in patients with AHP. We used an existing 'grip selection task', which investigates motor representations by comparing how patients would grasp an object and how they actually grasp the same object. Eight right hemisphere stroke patients with AHP, 10 control patients (non-AHP), and 22 age-matched healthy volunteers (HVs) completed the task. Results showed that HVs outperformed both AHP and non-AHP patients in their motor representations for the hemiplegic limb; however, the performance of AHP and non-AHP patients did not differ significantly. Motor representations for the intact limb were lower than normal in AHP patients, whereas performance in non-AHP patients was midway between the AHP and HV groups. Findings suggested that the ability to form motor representations lie on a continuum, but that impaired motor representations for the paralysed limb cannot account for AHP. Distorted motor representations, in combination with other deficits, might contribute to the pathogenesis of AHP.

Patients with a diagnosis of Parkinson's disease and age- and IQ-matched controls estimated the duration of short 500-Hz tones (325-1,225 ms), on trials where the tone was either preceded by 3 s of 5-Hz clicks, or presented without clicks. The click manipulation had been shown in earlier studies with student participants to make verbal estimates longer. Patients were tested both on and off their dopaminergic medication, and controls were also tested in two sessions. Verbal estimates were markedly and significantly longer on trials with clicks than on those without clicks for both the patients and the controls, but there were no significant performance differences between patients or controls, nor between the on and off medication sessions in the patients. The study shows that a manipulation of subjective time, which has had small but consistent effects in student participants, also affects timing in patients and adds to a growing body of evidence that timing in patients with Parkinson's disease may in many cases have the same characteristics as those of neurologically intact control groups.

Previous literature suggests that Parkinson's disease is marked by deficits in timed behaviour. However, the majority of studies of central timing mechanisms in patients with Parkinson's disease have used timing tasks with a motor component. Since the motor abnormalities are a defining feature of the condition, the status of timing in Parkinson's disease remains uncertain. Data are reported from patients with mild to moderate Parkinson's disease (both on and off medication) and age- and IQ-matched controls on a range of stimulus timing tasks without counting. Tasks used were temporal generalization, bisection, threshold determination, verbal estimation, and a memory for duration task. Performance of patients was generally "normal" on all tasks, but significant differences from performance of controls were found on the memory for duration task. Among the "normal" effects noted were arithmetic mean bisection, asymmetric temporal generalization gradients, and subjective shortening on the memory for duration task. The results suggest (a) that some previous reports of timing "deficits" in Parkinson's patients were possibly due to the use of tasks requiring a timed manual response and (b) small differences between patients and controls may be found on tasks where two stimuli are presented on each trial, whether patients are on medication or off it.

There is conflicting evidence about whether Parkinson's disease (PD) is associated with deficiencies in recognition memory (RM) and the processes which underlie it, namely recollection (a form of recall) and familiarity (a feeling of memory in the absence of recall). The aims of the current study were to examine forced-choice verbal RM (assessed with the Warrington Recognition memory Test), yes-no RM, recollection, familiarity and executive functioning in 17 patients with moderate PD and 17 healthy volunteers matched for age and premorbid intelligence. We predicted that patients with moderate PD would display a significant recollection deficit on the yes-no RM test, because their strategic memory processing that depends on executive functioning and is necessary for efficient encoding and/or retrieval, was disrupted. In contrast, familiarity memory, which is not dependent on these processes, and forced-choice RM (which is largely dependent on familiarity) should show higher levels of preservation. We also predicted that recollection should be correlated with severity of executive dysfunction. Our findings revealed that the PD patients were as likely to accurately discriminate between targets and distractors as the healthy volunteers on both RM tests. However, the PD patients were significantly less reliant on recollection-driven recognition decisions on the yes-no RM test when compared with the healthy control group. The patients also displayed executive function deficits, but these were not correlated with recollection. The extent to which the PD patients' reliance on familiarity at the expense of recollection is explained by impairments in strategic memory processes/executive function and/or medial temporal lobe retrieval processes needs further exploration.

In an earlier study we disputed the claim that the mediodorsal thalamic nucleus is critical for familiarity. We reported patient (QX) who showed a severe deficit in conscious recollection, and behavioural problems (disinhibition, emotional lability) with relative sparing of familiarity-aware memory following a left mediodorsal thalamic lesion. More recent MR imaging has revealed that QX's lesions are more extensive than previously reported and involve both dorsolateral thalamic nuclei, and whilst there is evidence of left mediodorsal thalamic damage, it is not the main focus of damage. This paper reports a full analysis of QX's thalamic pathology alongside a more detailed investigation of his recognition memory, using yes/no and forced-choice procedures, and executive function. The results revealed impairments in yes/no recognition and conscious recollection rates of famous, artist and unknown names. In addition to the previously noted behavioural disinhibition and emotional lability, a deficit in spontaneous planning ability was evident on the Zoo Map Test (subtest of the Bahavioural Assessment of the Dysexecutive Syndrome). Forced-choice recognition, familiarity estimates and remote memory showed higher levels of preservation. The findings indicate that the dorsolateral thalamus is part of the extended hippocampal circuit which is causally critical only for recall and conscious recollection of complex associations rather than for the more automatic processes linked with novelty detection.

Background: Dual-process models propose that recognition memory (RM) involves two processes: conscious recollection and familiarity-aware memory. Studies investigating RM in schizophrenia report a selective deficit in conscious recollection and intact levels of familiarity-driven RM for stimuli presented in the visual and olfactory domains. It has been suggested that abnormalities in conscious recollection result from a breakdown in frontal strategic memory processes involved in encoding and retrieval and executive functions linked to reality monitoring and decision making. We investigated three predictions arising from these proposals. Firstly, if conscious recollection abnormalities arise from a central impairment, then these abnormalities should not be domain specific. Secondly, if the deficits in conscious recollection arise from a breakdown in executive processes, deficiencies should be correlated with executive dysfunction. Finally, the conscious recollection deficiencies are likely to be more severe in schizophrenia, a condition associated with marked executive dysfunction relative to Major Depressive Disorder, Recurrent (MDDR), in which executive dysfunction is less marked., Methods: The remember/know paradigm was used to investigate RM for voices in three groups: patients with schizophrenia (n = 14), patients with MDDR (n = 16), and normal controls (n = 16). Executive function was assessed using the Wisconsin Card Sorting Task., Results: Patients with schizophrenia made significantly fewer remember responses than normal controls (p < 0.01), despite normal levels of discrimination and familiarity-driven auditory RM. Patients with MDDR did not differ significantly from either normal controls or patients with schizophrenia. Executive dysfunction was limited to the schizophrenia group and was not correlated with conscious recollection deficiencies., Conclusions: Patients with schizophrenia exhibit a deficit in conscious recollection for auditory RM of voices. These findings, when considered alongside remember/know data collected from the same set of patients for olfactory and visual RM, support proposals that abnormalities in conscious recollection stem from a breakdown in central rather than domain-specific processes., (Copyright 2006 S. Karger AG, Basel.)

We report findings from a cognitive neuropsychological and psychophysiological investigation of a patient who displayed an exacerbated acute emotional expression during movement, innocuous, and aversive somatosensory stimulation. The condition developed in the context of non-specific white matter ischaemia along with abnormalities in the cortical white matter of the left anterior parietal lobe, and subcortical white matter of the left Sylvian cortex. Cognitive neuropsychological assessment revealed a pronounced deficiency in executive function, relative to IQ, memory, attention, language and visual processing. Compared to a normal control group, the patient [EQ] displayed a significantly elevated skin conductance level during both innocuous and aversive somatosensory stimulation. His pain tolerance was also significantly reduced. Despite this, EQ remained able to accurately describe the form of stimulation taking place, and to rate the levels of pain intensity and pain affect. These results suggest that EQ's exaggerated behavioural response and reduced pain tolerance to somatosensory stimulation may be linked to cognitive changes, possibly related to increased apprehension and fear, rather than altered pain intensity or pain affect per se., (Copyright 2004 IOS Press)

Background: Recognition memory (RM) is impaired in patients with schizophrenia, as they rely largely on feelings of familiarity rather than conscious recollection. It has been suggested that this abnormality may reflect a breakdown in strategic memory processes involved in both encoding and retrieval. By studying 2 patients with false recognition (FR; patient C.T.) and delusional misidentification (DM; patient B.C.), and a group of psychotic control patients, we examined proposals that FR and DM exist on a continuum of increasingly severe impairment in strategic memory function., Methods: Executive function, autobiographical memory and verbal and facial RM were assessed using standard neuropsychological tests and the remember/know paradigm., Results: The psychotic control group displayed a significantly reduced reliance on remember judgements and compensatory elevation in know judgements on both RM tasks compared with the normal control group. Patient B.C. also followed this trend, but in a much more pronounced manner. In contrast, patient C.T. displayed a qualitatively different performance profile, which was marked by an increased dependence on remember responses., Conclusions: We have presented evidence which support proposals that a breakdown in strategic memory and executive dysfunction are more pronounced in DM than FR. However, the small sample size precludes any firm conclusions being drawn., (Copyright 2003 S. Karger AG, Basel)

Background: Recognition memory dysfunction has been frequently reported in schizophrenic populations, and has been linked with the development of delusions and thought disorder. A range of neuropsychological abnormalities have also been documented in the biological asymptomatic relatives of patients with schizophrenia; however, recognition memory has not been one of them., Aim: This study was carried out in order to investigate: (i) verbal and facial recognition memory in terms of accuracy and false alarm rates; and (ii) contributions from the episodic and semantic memory systems to recognition memory, in the biological asymptomatic parents of a reported schizophrenic patient and a set of male and female psychotic controls., Results: Gender differences failed to emerge between the psychotic controls on any of the recognition measures (discrimination accuracy, response bias, hit and false alarm rates, 'remember' and 'know' recognition memory decisions). However, there was evidence of recognition dysfunction in the female relative, and to a lesser extent, in the male. Both parent's recognition memory performance profiles were marked by a pathologically elevated false alarm rate, and an increased dependence 'remember' judgements, i.e. input from the episodic memory system, to drive recognition memory decisions., Conclusions: These findings are discussed in the context of models of episodic and semantic memory impairment in schizophrenia.

This study reports a patient with a unilateral left thalamic lesion which was centred on the dorsomedial thalamic nucleus. Cognitive neuropsychological assessment revealed a severe impairment in verbal memory and symptoms of executive dysfunction, in the presence of relatively intact visual and facial recognition, working memory, praxis, language and IQ. Verbal and visual recognition memory were investigated using the remember-know paradigm. The results indicated a profound impairment in recollection-driven verbal recognition memory. These results are discussed in the context of the role of the dorsomedial thalamic nucleus in recognition memory, and functional models of memory.

Previous neuropsychological studies have demonstrated an association between person misidentification and right-hemisphere dysfunction. In the study reported here, we explore the contribution of facial and visual recognition impairments in a patient with right-hemisphere subcortical white-matter pathology in the frontal and parietal lobes and a diagnosis of vascular cognitive impairment. The patient displayed false recognition of unfamiliar faces and deficient retrieval of key biographic detail for famous faces. These results are discussed in the context of the contribution of deficiencies in the visual system and subcortical white-matter lesions to the development of Capgras delusion., (Copyright 2002 S. Karger AG, Basel)

In this article the epidemiology, aetiology, neuroanatomy and neuropsychology of the Capgras syndrome (CS) are reviewed in detail. CS is characterized by the delusional belief that one or a few highly familiar people have been replaced by impostors who are physically very similar to the original/s. The patient acknowledges that the double and known person look alike, but maintains the belief that the significant person, in psychological terms, is absent. CS is relatively rare, occurring predominantly in the context of schizophrenia, and was traditionally considered to have its origins in psychodynamic conflict. More recently, however, it has been estimated that between 25 and 40% of cases are associated with organic disorders, which include dementia, head trauma, epilepsy and cerebrovascular disease. Neuroimaging evidence suggests a link between CS and right hemisphere abnormalities, particularly in the frontal and temporal regions. Neuropsychological research has provided empirical support for these findings, by consistently reporting the presence of impairments in facial processing--an established right hemisphere function. It is likely that the study of this symptom will lead to a greater understanding of the neurological basis of psychotic experiences and may provide a paradigm for how the psychoses should be investigated.

Background: The relationship between midline structural defects and schizophrenia remains unclear, although a number of neuroradiological studies have reported an association between schizophrenia and a range of anomalies., Method: Three patients are reported, each diagnosed with schizophrenia and neuroradiological evidence of midline structural anomalies. MRI scans are reported in conjunction with performance over a range of neuropsychological tests designed to assess frontal and lateralised cognitive functions., Results: Evidence of anterior dysfunction was present in all three cases, while on an individual basis patients displayed varying patterns of preserved and dysfunctional cognitive processing., Conclusion: The reported findings raise a number of interesting issues regarding the nature of hemispheric involvement in schizophrenia.

We investigated four paranoid schizophrenic patients diagnosed with Frégoli delusion, and four matched psychotic controls. Neuropsychological testing included visual and verbal recognition memory, in addition to a comparison of left and right hemispheric processing of two different classes of stimuli, animate and inanimate objects. Performance on the recognition memory test failed to discriminate between the two psychotic groups on the basis of facial recognition, however, the patients with Frégoli delusion failed to show the right hemisphere processing advantage for the animate class of stimuli found for the set of norms and also present in the psychotic control group. These results are discussed in the context of both current theories of the delusional misidentification syndromes in general, and models of facial recognition in particular.

The present study provides detailed anatomical evidence that the strongly texture-sensitive complex neurones of the cat's striate cortex constitute a discrete subset of all complex neurones, and lie in two bands, deep in lamina III and in lamina V. Physiological properties of simple and complex striate cortical neurones were characterized extracellularly in lightly anaesthetized cats by use of micropipettes filled with 12% Fast Green FCF dye in 2.0 M sodium chloride. Complex neurones were further subdivided on the basis of their length-summating properties for an optimally oriented bar into "standard," "special," or "intermediate" categories and on the basis of their tuning and degree of sensitivity to motion of random texture. Extracellular dye marks were made at strategic locations along each microelectrode track, especially at the site of recording from strongly texture-sensitive complex neurones. Tracks were reconstructed with the aid of the histologically recovered dye marks in sections counterstained with cresyl violet to reveal cortical lamination. The results confirm and refine the inference made by Hammond and MacKay (Exp. Brain Res. 22:427-430, '75; Exp. Brain Res. 30:275-296, '77) and the gross observations from 2-deoxyglucose uptake studies by Wagner, Hoffmann, and Zwerger (Brain Res. 224:31-43, '81) concerning the laminar distribution of texture-sensitive complex neurones in the cat's striate cortex.